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Testosterone: Functions and Regulation

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The intricate hormonal interplay essential for male reproductive health begins with the release of gonadotropin-releasing hormone (GnRH) by the hypothalamus. This hormone prompts the pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH targets the Leydig cells in the testes, stimulating them to produce and release testosterone. In concert with testosterone, FSH acts on the Sertoli cells within the seminiferous tubules to facilitate the release of...

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Related Experiment Video

Updated: Feb 17, 2026

A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl

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Published on: November 28, 2014

Testosterone regulates granzyme K expression in rat testes.

Dibyendu Dutta¹, In Park¹, Hiwot Guililat¹

¹.

Endocrine Regulations

|December 13, 2017

Summary

This summary is machine-generated.

Testosterone depletion increases germ cell apoptosis and Granzyme K (GZMK) expression in testes. GZMK may indirectly regulate apoptosis by affecting spermatid release, suggesting a role in male reproductive health.

Keywords:

apoptosis blood-testis barrier epididymis ethylene dimethane sulfonate round spermatids transition protein 1

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Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Published on: February 8, 2016

Area of Science:

Reproductive Biology
Molecular Endocrinology
Cell Biology

Background:

Testosterone depletion is known to increase germ cell apoptosis in the testes.
The specific genes regulating germ cell apoptosis under these conditions are not well understood.
Granzymes (GZM) are serine proteases involved in apoptosis, with several variants present in the testes.

Purpose of the Study:

To investigate which granzyme (GZM) variant is testosterone-responsive.
To determine the potential role of testosterone-responsive granzymes in germ cell apoptosis following testosterone depletion.

Main Methods:

Testosterone depletion was induced in rats using Ethylene Dimethane Sulfonate (EDS) to ablate Leydig cells.
Testosterone levels were confirmed via radioimmunoassay.
Granzyme variant mRNA expression was quantified using qPCR.
Germ cell apoptosis was assessed by TUNEL assay, and GZMK localization by immunohistochemistry.

Main Results:

EDS treatment successfully depleted serum and testicular testosterone.
A significant reduction in testis weight (18%) and increased germ cell apoptosis were observed 7 days post-EDS.
Granzyme K (GZMK) expression was elevated and localized to spermatid cytoplasm, not directly to apoptotic cells.
Apoptotic round spermatids were found in the caput epididymis.

Conclusions:

Granzyme K (GZMK) expression in the testes is dependent on testosterone levels.
GZMK's localization suggests a role in the degradation of microtubules within ectoplasmic specializations.
Overexpression of GZMK may indirectly contribute to germ cell apoptosis by promoting the premature release of round spermatids.